Hematology & Coagulation
Interactive clinical decision-making simulation (choose-your-own-adventure)
Objectives
Tip: Use Tab to move between options and Enter/Space to select.
A 55-year-old male is in the ICU for septic shock secondary to pneumonia, ICU day #3. He is intubated and mechanically ventilated, receiving norepinephrine at 0.18 mcg/kg/min.
"He’s bleeding from IV sites, has blood in his urine, and petechiae on his chest."
What is your initial approach to this deteriorating patient?
⚠️ Immediate stabilization helps, but you still need the “why”
Empiric products may temporarily reduce bleeding, but without identifying the underlying defect you risk under- or over-treating. In DIC, for example, ongoing consumption continues until the trigger is controlled.
✓ Best first step
You need data before targeted treatment. The presentation suggests a consumptive coagulopathy, but important alternatives include HIT, TTP, and HUS.
⚠️ Consequence branch: anticoagulation worsens bleeding
You treat as HIT and start argatroban. Within 30 minutes, oozing increases at IV sites and hematuria worsens. HIT is typically thrombotic, not hemorrhagic.
⚠️ Consequence branch: unstable transport risk
During transport, MAP drops to 52 despite pressor escalation. You return to the ICU and stabilize first. The bleeding pattern looks diffuse/systemic rather than a focal source.
- Diffuse bleeding and thrombocytopenia in sepsis → systemic coagulopathy likely.
- Workup must distinguish DIC vs TTP/HUS vs HIT (different treatments).
Which laboratory studies do you order? Select all that apply.
Select labs, then submit.
⚠️ Consequence branch: critical data gap delays care
✓ Appropriate workup ordered
Excellent. You ordered the essential evaluation to differentiate ICU coagulopathies and guide transfusion. (This aligns with Week 2 objectives: differentiate HIT/HUS/TTP/DIC and use TEG to guide management.)
- You ordered a coagulopathy workup including TEG/ROTEM and fibrinogen.
- You obtained type & screen to support safe transfusion if needed.
Which diagnosis best explains this pattern?
✓ Correct: DIC
Classic DIC: thrombocytopenia + prolonged PT/aPTT + low fibrinogen + elevated D-dimer in the context of sepsis.
⚠️ Consequence branch: treating HIT increases hemorrhage risk
You treat as HIT and start therapeutic argatroban. Because PT/aPTT and fibrinogen are not typically abnormal in HIT, this decision does not address the underlying problem and can worsen bleeding.
- 1 hour later: oozing increases; hematuria persists.
- Repeat labs: fibrinogen remains low; PT/aPTT remain prolonged.
⚠️ Consequence branch: delaying plasma exchange in presumed TTP
You treat as TTP and call for emergent plasma exchange. While mobilizing PLEX, hematology points out that PT/aPTT are prolonged and fibrinogen is very low—findings that typically argue against TTP and toward DIC.
- Delay: 2 hours spent arranging PLEX while bleeding continues.
- Peripheral smear shows only rare schistocytes; haptoglobin is normal.
⚠️ Consequence branch: supportive HUS focus misses consumptive coagulopathy
You treat as HUS and focus on renal support. However, HUS typically has normal PT/aPTT and normal fibrinogen. Meanwhile, the patient’s bleeding worsens.
- Bleeding from lines continues; Hb drops 1.5 g/dL.
- Sepsis persists; coagulation abnormalities remain global.
⚠️ Consequence branch: attributing to liver disease misses acute DIC
You attribute abnormalities to liver failure and plan vitamin K/FFP. The team reviews trend data: platelets fell from 165k to 38k rapidly, fibrinogen is critically low, and D-dimer is markedly elevated in sepsis—this is much more consistent with DIC.
Treat the underlying cause. In sepsis-associated DIC, source control + antibiotics + shock support are essential. Blood products address bleeding or procedure risk—do not transfuse solely to normalize labs.
What are your immediate management priorities? Select all that apply.
- R time reflects clot initiation (coagulation factors) → prolonged suggests factor replacement (FFP).
- K time / α angle reflect clot kinetics (fibrinogen) → abnormal suggests cryoprecipitate.
- MA reflects clot strength (platelets ± fibrin) → low suggests platelets.
- LY30 reflects fibrinolysis → high suggests TXA (not present here).
Based on these TEG results, which blood products are indicated? Select all that apply.
Platelets: 72,000 (↑) • Fibrinogen: 160 (↑) • INR: 1.6 (↓) • Bleeding: resolved • Pressors: decreasing
What is the most important ongoing management step?
✓ Correct
DIC resolves only when the underlying cause is controlled. Continue antibiotics, pursue source control, and support hemodynamics/oxygenation.
⚠️ Consequence branch: recurrent bleeding
Therapeutic anticoagulation in bleeding-predominant DIC can precipitate recurrent hemorrhage. DVT prophylaxis may be considered later once bleeding risk is controlled.
⚠️ Consequence branch: transfusion-related harm
Transfusing to “normalize labs” can cause volume overload, TRALI, and thrombosis. In DIC, transfuse for bleeding, procedures, or functional deficits—not numbers alone.
⚠️ Consequence branch: no targeted benefit
Corticosteroids are not a DIC-specific treatment. They do not correct consumptive coagulopathy and may worsen infection control.
Sepsis-associated Disseminated Intravascular Coagulation (bleeding phenotype)
- Bleeding controlled with goal-directed products
- Shock improved with antibiotics + source control
- Coagulation parameters improved as sepsis resolved
- Eventually transferred out of ICU
- Stabilize and order a focused coagulopathy evaluation.
- Use labs to distinguish DIC from HIT/TTP/HUS.
- Treat the underlying trigger (sepsis) while managing bleeding risk.
- Use TEG to guide targeted transfusion (FFP/Cryo/Platelets).